What is the clinical evidence from this study?

Study design: Other. Intervention: Aconitine. Primary outcome: Inhibition of ultrarapid-delayed rectifier K(+) current (I(Kur)).

What question did this study set out to answer?

This study aims to explore the effects of Aconitine on ultrarapid-delayed rectifier K+ currents in heart-derived cells.

September 8, 2008Toxicological Sciences

Time-Dependent Block of Ultrarapid-Delayed Rectifier K+ Currents by Aconitine, a Potent Cardiotoxin, in Heart-Derived H9c2 Myoblasts and in Neonatal Rat Ventricular Myocytes

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Key result

Aconitine suppressed ultrarapid-delayed rectifier K+ current in a time- and concentration-dependent manner in cardiac myocytes, with an IC50 of 1.4 microM.

Population

Differentiated clonal cardiac (H9c2) cells and cultured neonatal rat ventricular myocytes

Design

Preclinical

Authors

YWYa‐Jean WangMinghsin University of Science and Technology BCBing-Shuo ChenBeijing University of Technology MLMing‐Wei LinKaohsiung Medical University

Discussion

Member takes

Implication

Aconitine may promote cardiotoxicity via IKur blockade; leaves open human arrhythmogenic relevance.

Key Points

This study aims to explore the effects of Aconitine on ultrarapid-delayed rectifier K+ currents in heart-derived cells.
Investigated the impact of Aconitine on ion currents in H9c2 cells and neonatal rat ventricular myocytes.
Measured the concentration-dependent blockade and inactivation of I(Kur) using electrophysiological techniques.
Conducted single-cell Ca(2+) imaging and multielectrode recordings to assess the physiological effects of Aconitine.
Aconitine inhibited I(Kur) with an IC(50) of 1.4 microM in H9c2 cells.
In neonatal rat ventricular myocytes, Aconitine prolonged action potentials and induced early afterdepolarizations.
Aconitine altered electrocardiographic signals in neonatal rat tissues, correlating with I(Kur) inhibition.

Structured PICO

Population

Differentiated clonal cardiac (H9c2) cells and cultured neonatal rat ventricular myocytes

Intervention

Aconitine (ACO)

Outcome

Ultrarapid-delayed rectifier K(+) current (I(Kur))surrogate

Aconitine exerts cardiotoxic effects by blocking ultrarapid-delayed rectifier K+ currents, leading to action potential prolongation and early afterdepolarizations.

Cite This Study

Wang et al. (2008) studied this question. Aconitine was evaluated on Inhibition of ultrarapid-delayed rectifier K(+) current (I(Kur)). Aconitine suppressed ultrarapid-delayed rectifier K+ current in a time- and concentration-dependent manner in cardiac myocytes, with an IC50 of 1.4 microM.

synapsesocial.com/papers/6a2253453dc1edca6bb60048 https://doi.org/10.1093/toxsci/kfn189

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Time-Dependent Block of Ultrarapid-Delayed Rectifier K+ Currents by Aconitine, a Potent Cardiotoxin, in Heart-Derived H9c2 Myoblasts and in Neonatal Rat Ventricular Myocytes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Time-Dependent Block of Ultrarapid-Delayed Rectifier K+ Currents by Aconitine, a Potent Cardiotoxin, in Heart-Derived H9c2 Myoblasts and in Neonatal Rat Ventricular Myocytes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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